Understanding, Detecting, and Managing the Risk of Posttraumatic Osteoarthritis Following Anterior Cruciate Ligament Reconstruction in the Military

Anterior cruciate ligament (ACL) injuries occur approximately 4 to 5 times more frequently among active duty military personnel [1] compared to the general public [2, 3]. While 90% of individuals return to active duty following ACL reconstruction (ACLR) [4], approximately one-third of all individuals will develop posttraumatic osteoarthritis (PTOA) within the first decade following ACLR, and approximately 50% of individuals will develop PTOA within 2 decades following ACLR [5]. Osteoarthritis is the second leading cause of military discharge during armed conflict [6], and approximately 35% of all knee osteoarthritis cases in the military occur following a joint injury [7]. PTOA was the cause of end-stage joint disease in 75% of knees in a cohort (N = 64) of young military personnel (≤50 years old) undergoing total knee arthroplasty [8]. ACL injuries have devastating long-term effects on quality of life, which negatively impact the career longevity for many military personnel. Unfortunately, there are no current disease-modifying interventions for PTOA; thereby, prevention of PTOA onset following joint injury is critical for maintaining long-term health. Therefore, in addition to returning patients to unrestricted physical activity, clinicians should focus on early detection of PTOA development and management of PTOA risk in patients following ACLR.

As early as 4 years following an ACLR, individuals with a unilateral ACLR demonstrate greater radiographic tibiofemoral joint space narrowing on the ACLR limb compared to the contralateral limb [9]. However, deleterious changes in joint tissue metabolism occur within days to weeks of ACL injury and ACLR [10]. Relying on traditional radiographic evaluation of structural joint changes may not detect the early tissue changes that occur at a molecular level, which may lead to PTOA onset. Decreased proteoglycan density of the tibiofemoral articular cartilage has been demonstrated within the first 24 months following ACLR using novel T1ρ magnetic resonance imaging [11-13]. Patient-reported function can be used to detect individuals who demonstrate poor outcomes following ACLR.

Approximately 43% and 39% of ACLR patients report unacceptable outcomes using cutoff values derived from the Knee Injury and Osteoarthritis Outcomes Score [14] at 2 (N = 1530) and 6-year (N = 1506) follow-up exams, respectively [15]. Functional screening of slow habitual walking speed has been used to predict those who will develop idiopathic osteoarthritis [16]. In a cohort of older individuals at risk for developing osteoarthritis, a 0.1 m/s decrease in habitual walking speed over a 12-month period was associated with an 8% increased risk of developing radiographic osteoarthritis in the subsequent 24-months [17]. In younger individuals with an ACLR, slower walking speeds associate with greater concentrations of serum biomarkers of collagen breakdown [18]. Therefore, future efforts to detect early PTOA may need to focus on early compositional tissue alterations, as well as clinical changes in patient-reported function and activities of daily living, such as habitual walking speed.

Management of PTOA risk should begin prior to the development of the earliest signs or symptoms in order to maximize long-term joint health following ACLR. It is important that ACLR patients are educated regarding the risk of PTOA following ACL injury and current options for managing the increased risk of developing a chronic disease. A recent study evaluating how certified athletic trainers perceive and manage the risk of PTOA found that while 97% of healthcare professionals agree that ACL patients should be educated about their increased risk of PTOA following ACLR, only 71% of healthcare professionals actually report explaining this risk to their patients [19]. In a separate study, only 27% of patients with an ACLR reported that a healthcare professional explained risk of PTOA following ACLR, which may explain why most patients believe that ACLR will decrease the risk of PTOA, and only 7% of ACLR patients from the United States believed that developing osteoarthritis was a major healthcare concern [20]. In addition to education, proper movement biomechanics and adequate lower extremity muscle strength should be developed and maintained to decrease the risk of a second traumatic knee injury and chronic aberrant mechanical loading of the ACLR knee. Specifically, quadriceps weakness is associated with increased odds of developing osteoarthritis [21], as well as greater tibiofemoral joint space narrowing [22] and worse self-reported function following ACLR [23]. Clinical efforts should be made to maximize quadriceps strength to achieve inter-limb symmetry and an adequate amount of bilateral strength relative to the individual's body weight [23]. Furthermore, increased disability is often coupled with an increase in non-lean bodyweight following knee injury [24]. Efforts to maintain a healthy bodyweight following ACLR may directly minimize aberrant mechanical loading to the knee [25] and indirectly minimize the potential adverse effects that increased circulating adipocytokines may have on systemic joint inflammation [26]. Finally, it is important that patient education, muscle strengthening, and weight management are managed on a continual basis, and serial assessments of PTOA risk should be conducted even after patients have returned to normal physical activity or active duty.

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